Provide a definition of health, illness and disease and describe various ways to quantify each

Identify the multiple genetic and environmental determinants of health and describe how virtually all outcomes result from their combined effects

Explain how an individual’s adaptation to stress, or lack thereof, influences the full range of health outcomes

Describe the ways in which physicians can and cannot affect the major determinants of health

Color Key

Important key words or phrases.

Important concepts or main ideas.

1. Introduction

What makes people sick? What ever it is be glad for it.
Medical school would otherwise be a big mistake.

When it comes to illness, physicians deal far
more with the consequences than with the causes.We don’t generally probe
deep enough to find out why our patients are sick. Say, for example, a
patient suddenly develops slurred speech and weakness in her right arm and leg.
We would routinely diagnose a stroke and begin to treat to her. We usually
explore a little further and find out that the stroke most likely resulted from
long-standing hypertension and atherosclerosis. Sometimes our investigation
ends there, though often we go on to inquire about the patient’s
lifestyle and family history to see how they may have contributed to her high
blood pressure and serum cholesterol levels. Then we stop. We generally
don’t ask, for example, what accounted for her high fat diet, cigarette
smoking, lack of exercise or genetic predisposition to cerebrovascular disease.
In other words, we focus on the proximal associations rather than underlying
etiologies of disease. We rarely try to get to the bottom of the problem.

This is not out of laziness or apathy.
There are good reasons why we can often only scratch the surface. What are
they? Why not dig deeper?

2. Are you healthy?

Before we can discuss the determinants of health, we
need to consider what health is and how to measure it.

Assume for a moment you are healthy (which your probably
are.) Why? What does it take to be healthy? This is no idle philosophical
exercise. If you don’t know what it looks like, how are you going to
recognize health when you see it in your patients? If health were simply the
absence of disease, life would be easy. Identifying relatively disease is easy,
defining health is not.

A patient comes in complaining of fatigue.
You find nothing wrong. At what point would tell him he’s healthy? The
next patient comes in for a routine physical. She feels fine. What information
would you need before you declared her healthy?

For the most part, physicians are
trained to identify and treat disease. That’s when we
are most comfortable. Sometimes, however, the exclusive pursuit
of disease can become a negative determinant of health. A
“healthy” patient with no obvious disease, for example, may undergo
multiple screening tests to look for one. Preventive medicine
is based largely on the principle that disease often masquerades as health, and
physicians ought to inform their patients that they are not as healthy as they
may think. While identifying a life threatening disease before it becomes
symptomatic can be of great benefit to a patient, care must be taken not to
pursue an asymptomatic disease when there’s no reasonable chance of
finding it.Looking for a disease in a “healthy
person” can sometimes harm them.

2.1. Measuring Health Outcomes

Our definition of
health influences how we measure it. Being able to reliably
measure health is important for at least three reasons.

First, it makes it possible to follow your
patients’ progress over time and determine whether they still need your
care.

Second, in order to pay for medical
products and services, it is necessary to assign some value to a quantifiable
unit of health.

And third, well-defined health measures
are necessary to conduct epidemiologic and clinical research, without which we
could not practice scientifically-based medicine (the subject
of a subsequent lecture).

Death, of course, is the ultimate measure of poor
health. Mortality rates are particularly useful when it comes to measuring the
health of a population, but clinicians understandably prefer to rely on other
(more reversible) health indicators. Morbidity, a term often
used by epidemiologists to describe the burden of disease in a population, is
expressed as the incidence or prevalence of a diagnosable condition of
interest. In a clinical context, morbidity generally refers to disease states
having serious medical implications. While this is a useful measure of a
disease’s existence, and to some degree its severity, it says little
about the impact it has on a patient’s overall health. The most
useful health measures capture a patient’s level of disability or the
quality of their life. Since they are more subjective, however, disability and
quality of life are more difficult to quantify and compare, compromising their
usefulness, particular in research.

Another way to think about measures of
health outcomes is to divide them into two types:
disease-oriented and patient-oriented. As
the name implies, disease-oriented outcomes reflect the status of a disease
process, which may or may not be of immediate concern to the patient.
Let’s return to our stoke patient. If a researcher wanted to know whether
or not a drug is more effective than a placebo at treating hypertension, the
most expedient outcome to measure would be blood pressure. Such a study can be
carried out in a matter of months. What ultimately matters, however, is not the
patient’s blood pressure but whether or not the medication prevents the
major complication of hypertension, namely stroke.

To determine this, researchers would need to follow
subjects far longer and in greater numbers to see if the medication could
effectively lower the risk of stroke. While blood pressure
reduction is disease-oriented, stroke risk reduction is
patient-oriented. Even though, out of necessity, most clinical
research is disease-oriented, physicians often extrapolate data from large
epidemiologic studies, which suggest that the average stroke rate in
populations with uncontrolled hypertension is higher than in normotensive
populations. Due to the well-known flaws inherent in epidemiologic studies, of
course, these assumptions may prove to be incorrect.

Always remember, it is the patient-oriented
outcome that matters most. Physicians spend their days diagnosing,
treating and preventing diseases. Our patients, on the other hand, suffer
illnesses, which represents their perception of a disease process – if
one exists. While the medical view of their disease often overlaps with the
patients’ experience of it, in many cases there is little correlation
between the two. By focusing our attention exclusively on disease, we may miss
our patients’ illnesses.

Can you think of a situation where you
might identify a disease where there is no illness? How about the reverse, an
illness with no disease?

3. What Determines Health?

This is an extraordinarily complex question, one that
does not lend itself to our customary way of linear thinking. Sometimes event A
does lead directly to health outcome B. In most cases, however, this simple
relationship does not exist. When a basketball player, for example, twists his
ankle after landing on another player’s foot following a rebound, it is
clear that the forceful inversion of his foot tore the fibers in one or more
ligaments leading to an ankle sprain. This simple cause and effect
relationship, however, would never apply to a patient arriving in the emergency
department with crushing chest pain from a myocardial infarction. While there
may be a straightforward linear relationship between the sudden thrombosis
(blood clot) of a coronary artery and death of myocardial tissue, the
aggregation of factors leading up to that event is complicated, obscure and
impossible to know for certain. We do know, however, that on that day numerous
conditions in the patient’s past combined in such a way as to increase
his probably of a having myocardial infarction to 100%. These conditions could
have occurred as long as ago as 100,000 years or as recent as breakfast that
morning. As the time separating two events increases, it becomes more
difficult to formulate linear associations between them, let alone do anything
to change their interaction. This is why in medicine,
the more recent the predisposing condition or risk factor, the more attention
we pay to it.

It is possible to obtain some insights into
these complex relationships by viewing various health determinants along a
timeline. As a species we are prone to experience certain health
outcomes under a given set of conditions due to our evolutionary history. Some
have argued, in fact, that the existence of virtually all human disease
ultimately has an evolutionary explanation (all of which, by the way, are
difficult if not impossible to test). On an individual level, the genes we
inherit transmit this evolutionary vulnerability from one generation to the
next. While we will never be able to change out evolutionary history, some
believe we are rapidly approaching a time when will be able to change our
genetic inheritance.

Let’s assume, for the time being, that we come
with a fixed genome. This package of genes predisposes each of us to specific
health outcomes – good and bad. Over a lifetime, these genes encounter a
range of environmental conditions (some quite extreme) along with opportunities
for adaptation (some quite limited). While some genes are relatively stable,
others show considerable plasticity, switching on and off in response to
constantly changing environments. The vast majority of our
health outcomes are a manifestation of our genetically-influenced response to
the nature and timing of these environmental exposures.

Depending on our genome, one environmental hit at a
vulnerable time can have a greater impact on long-term health than multiple
hits over decades. Witnessing a tragic event in early childhood, for example,
may lead to decades of ill health, while smoking a pack of cigarettes a day for
sixty years may produce no discernable health consequences. As you can see,
in virtually all cases it is neither nature nor nurture. It’s
both.

4. Environmental Determinants

Listed below are the major environmental determinants of
health:

Lifestyle choices or health behaviors

Pathogenic or toxic exposures

Health care

Socioeconomic status

Stress

While you will often see them listed separately,
it is impossible to isolate the influence of one determinant from all
the others. Take health behaviors as an example. Individuals who
practice destructive behaviors like smoking, overeating or excessive drinking
are often assumed to do so out of choice. They continue these behaviors despite
their risk either because they don’t know better, or they know the risks
but choose to ignore them. Or so the story goes. This kind of
oversimplification, based on proximal notions of cause and effect, is not only
naïve but potentially harmful. Physicians may wrongly decide that in order for
patients to adopt healthful lifestyles, they simply need to be educated. Or
even worse, they may blame these individuals for their unhealthful habits and
the illnesses they cause. The truth is, health behaviors are the end
result of complex interactions between multiple factors, many of which will
never be identified or addressed in the clinical setting.

If you had to choose one of the five
determinants listed above, which do you think has the broadest affect on health
outcomes? Where would you rank the relative influence of health
care?

4.1. Socioeconomic Status and Health

There is little debate that
socioeconomic status (SES) has a profound affect on
health. You needed look any further than developing countries to see
how abject poverty leads to high infant mortality rates and low life
expectancy. Until recently, it was assumed that once a country was able to meet
the basic human needs of the majority of its population, the health status of
most citizens would be roughly the same, particular in countries where access
to medical services is fairly uniform. But numerous
epidemiologic studies over the past 25 years have shown that a continuous
gradient, rather than a single threshold effect, describes the association
between SES and health, even in populations well-above the poverty
line. In societies able to meet the basic health needs of its
citizens – plentiful sources of safe food and drinking water, effective
sanitations systems, a public health infrastructure and ready access to
clinical services – the health of individuals occupying adjacent
socioeconomic stations will differ. And, for the most part, this phenomenon is
condition-independent; even slightly higher SES means lower
mortality and morbidity from the vast majority of chronic
diseases.

There are only a handful of conditions
whose prevalence increases with affluence. Can you think of any examples?

What still remains a mystery is how exactly this SES
gradient translates into health outcomes. So far, none of the various markers
commonly used to measure SES – income, education, job status and
neighborhood – has adequately explained the association, alone or in
combination. This suggests that there is at least one other underlying factor
common to both SES and health yet to be identified. One possibility has to do
with concept of social divisiveness.
Accumulating evidence suggests that a reliable predictor of the
health status of a society is how its members treat each
other.This may partly explain why we Americans are not
as healthy as we are wealthy. Hierarchical societies sharply divided
along class lines, like in the United States, tend to have higher infant
mortality rates and lower life expectancies, then more egalitarian societies
like in Sweden. According to this model, what matters is not the
uneven distribution of material resources, but the harmful psychosocial
consequences of a society that tolerates – even encourages – the
alienation of social classes.

4.2. Stress and Health

While this model provides a intriguing
and plausible explanation for the link between SES and health, it fails to
identify the mechanism by which social divisiveness actually leads to poor
health. Hypertension, for example, is more common in African
Americans than whites, and it is certainly conceivable that the long history of
slavery and racism in this country contributes to this disparity. Even if this
turns out to be true, what we still don’t know is exactly how racism
raises blood pressure. Adaptation to stress may be one possibility.

Imagine for a moment that you are living in the Stone
Age, some 10,000 years ago. Your day largely consists of gathering food for
your family to eat. Life is stressful, but you know how to survive, and you
take pride in your ability to handle whatever comes your way. Now imagine that
it is dusk, and you and some companions are returning home from a long,
exhausting day of hunting. You suddenly encounter a small pack of startled
wolves obviously threatened by your presence. A violent confrontation is
imminent, and to survive, you must quickly assess the situation and prepare to
take action. You and your companions know exactly what to do. You reflexively
coordinate your positions, ominously raise your weapons and prepare for a
fight. Unconsciously, your neuroendocrine system springs into action. A rapid
surge in epinephrine and cortisol from the adrenal glands sets in motion a
widespread set of physiologic changes coordinated to enhance your chances of
survival.

The standoff continues for about a minute before the
wolves retreat. As the danger subsides, so does the stress
response, which is highly adaptable to a rapidly changing
environment. As quickly as it turns on, it turns off once the
threat has passed. You proceed home, a little shaken, but otherwise feeling
fine as your stress hormone levels return to normal.

This scenario makes two important points.

First, stress is normal.
For our entire evolutionary history life on earth has been stressful, and the
fact that we are here to talk about it means we have successfully adapted to
it. Even today there are many examples where stress produces a
positive, or adaptive, effect. You already know that a certain level
of stress prior to an exam, for example, tends to enhance performance. You also
know that stress can have the opposite effect, leading to disastrous
consequences.

This raises the second point, stress is
adaptive only in so far as it is contained and appropriate to the
situation. Our prehistoric counterpart presumably lived on to
fight another day because he or she was able to mount the stress response
quickly and appropriately, and then extinguish it just as fast.

Here’s the problem. While the
physiology of this fight-or-flight response presumably hasn’t changed
much in thousands of years, our behavioral response has changed
dramatically. Often the result is a full blown fight or flight
response with nowhere to go – we neither fight nor fly. And, while we may
never encounter the random pack of wolves, we still confront major stressors,
many of which occur frequently or even continuously over a lifetime.
Repeatedly taking stressful hits without the opportunity for an
adaptive behavioral response translates into a continuous barrage of
stress-related hormones and neurotransmitters. Considerable
experimental evidence suggest that the accumulated effects of this
psycho-physiological reaction, referred to as allostatic
load, leads to widespread damage in virtually every organ system in
the body, and is probably involved in the pathogenesis of most chronic
diseases.

Chronic stress can contribute to
allostatic load in two ways: physiologic and
behavioral. In those individuals genetically predisposed to
vascular disease, for example, chronic exposure to the neuroendocrine products
of stress may lead directly to the development of hypertension and accelerated
atherosclerosis. And maladaptive behaviors associated with psychological stress
– tobacco use, excessive alcohol consumption, unhealthful diets and
non-compliance with anti-hypertensive medications – can clearly
exacerbate a genetic tendency toward hypertension and stroke.

It is important to keep in mind that stress is
not the problem. It’s the maladaptive response to stress that leads to
disease. Physiologists use the term stress to describe any
environmental exposure that challenges an organism’s
homeostasis. A more useful definition of stress for our
purposes is a psychological response to a perceived environmental
challenge, real or not, that a person feels incapable of coping
with.Perception is key. While some situations
are universally stressful (loss of a loved one, for example), in most
cases the experience of stress has far less to do with the stressor than with
an individual’s adaptability to psychological and physical
challenges.One person’s stressor is another
person’s opportunity.

4.2.1. Stress Management

There are three basic ways to avoid
the damaging effects of stress.

4.2.1.1. Eliminate or minimize stress in the first
place

The first is to endeavor to eliminate, or at least
minimize, stressful exposures in the first place. Even if this were possible,
spending energy on trying to escape life’s inevitable challenges is
wasteful and self-defeating. The problem, after all, is not the
stressor; it is the inability to adapt to it.

4.2.1.2. Respond to stress immediately

The second approach is to deal with the stress
response once it occurs. This is most commonly accomplished
with drugs. Medications like benzodiazepines effectively blunt
the perception of stress, but there is no evidence that they diminish its
damaging effects over time. β-blockers
are a class of medications that directly interfere with sympathetic stimulation
throughout the body, and unlike benzodiazepines, β-blockers have been shown to decrease the
damaging effects of stress on the cardiovascular system. Finally, various
mind-body interventions can permit patients to gain access to, and control
over, their own autonomic nervous system. While there is considerable
experimental evidence that techniques like meditation and biofeedback can
affect stress physiology, there is little clinical or epidemiologic evidence
that these interventions actually lead to favorable health outcomes over the
long-term.

4.2.1.3. Learn ot constructively adapt to
stress

The third option, which lies between the first
two, is to help patients constructively adapt to the inevitable stressors they
are sure to encounter. This approach makes a lot of sense, since
stress is ultimately a problem of adaptation, rather than simply a
physiologic response to an environmental exposure.
Cognitive-behavioral therapy (CBT) is probably the best
known and most widely studied method for influencing stress adaptability.
Recognizing that maladaptive stress responses involve harmful attitudes and
behaviors, cognitive-behavioral therapists help patients think differently
about their stressful encounters and act in a way to promote health. While CBT
has been used extensively in treating psychiatric diagnoses, its use in the
prevention and management of medical conditions is a relatively new
application.

5. Affecting Health Determinants

Given the enormous complexity of health and its
determinants, what can a linear-thinking, busy clinician realistically expect
to achieve? Oftentimes, a simple intervention is enough. Putting an ace wrap on
a sprained ankle and taping it up before the next game is all there is to do.
At other times, we can only scratch the surface of what’s really going
on. While we cannot be reasonably expected to recognize, let alone manage,
every possible health determinant, we can always ask these
three questions for every patient we see:

Why is my patient sick?
What
can I realistically do about
it?And,
if I can’t help, who can?

Let’s turn one last time to our stroke patient. By
the time you leave medical school it will become clear what you are expected to
do for patients like this. Manage the hypertension and respond to the stroke
when and if it occurs. This is the minimum. How much farther you decide to go
is your call.